1994
DOI: 10.1038/368703a0
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Elevated blood pressure and craniofaclal abnormalities in mice deficient in endothelin-1

Abstract: The endothelin-1 (ET-1) gene was disrupted in mouse embryonic stem cells by homologous recombination to generate mice deficient in ET-1. These ET-1-/- homozygous mice die of respiratory failure at birth and have morphological abnormalities of the pharyngeal-arch-derived craniofacial tissues and organs. ET-1+/- heterozygous mice, which produce lower levels of ET-1 than wild-type mice, develop elevated blood pressure. These results suggest that ET-1 is essential for normal mouse development and may also play a p… Show more

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Cited by 957 publications
(584 citation statements)
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“…Knockout studies indicated a role for ET-1 in bone formation since ET-1 null mice exhibit hypoplasia of the facial bones. ET-1 null mice die shortly after birth from respiratory failure and cardiac abnormalities [30]. Also serum ET-1 levels are increased in patients with bone osteoblastic lesions [31].…”
Section: Osteoblastic Bone Metastasismentioning
confidence: 99%
“…Knockout studies indicated a role for ET-1 in bone formation since ET-1 null mice exhibit hypoplasia of the facial bones. ET-1 null mice die shortly after birth from respiratory failure and cardiac abnormalities [30]. Also serum ET-1 levels are increased in patients with bone osteoblastic lesions [31].…”
Section: Osteoblastic Bone Metastasismentioning
confidence: 99%
“…Further transformations about the hinge are seen with the targeted disruption of both the endothelin signaling pathway and its potential targets, the nested Dlx5 and Dlx6 genes (Kurihara et al, 1994;Clouthier et al, 1998;Yanagisawa et al, 1998;Acampora et al, 1999;Depew et al, 1999;Charite et al, 2001;Ruest et al, 2004). Dlx5 is expressed both in early head mesenchyme (mdBA1 CNC) and epithelia (e.g., the early anterior cephalic ectoderm, ANR, and olfactory and otic placodes; Simeone et al, 1994;Qiu et al, 1997;Yang et al, 1998;Depew et al, 1999).…”
Section: Figmentioning
confidence: 99%
“…Evidence from EDN1 genetic mutants shows that ET and its converting enzyme are necessary for correct vascular development in the embryo. [68][69][70] Huang et al 71 reported that the EDN1 gene was directly involved in hypertension, and polymorphisms in the gene encoding ET receptor-A have been shown to be associated with essential hypertension testifying to the necessity of balance within the system for normal functioning in vascular tissues. 72 While we have reported on the importance of ET-1 expression in retinal microvasculature in high glucose, 73 there appears to be a lack of association between a polymorphism in the EDN1 gene and diabetic retinopathy after correction.…”
Section: Mhc and Immunity Markersmentioning
confidence: 99%